Autophagy induces apoptosis and death of T lymphocytes in the spleen of pigs infected with CSFV

Gou, Hongchao; Zhao, Mingqiu; Fan, Songqing; Yuan, Jing; Liao, J. W.; He, Wencheng; Xu, Hui; Chen, Jinding

doi:10.1038/s41598-017-14082-9

Cited by 20 publications

(17 citation statements)

References 50 publications

(81 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Apoptosis, autophagy, and pyroptosis are three main cellular biological processes with significant differences in their molecular mechanisms. However, these three cellular biological processes are not independent biological processes, but have potential interaction mechanisms [25,[82][83][84]. Therefore, in future studies, it is necessary to further reveal the mechanistic interplay between apoptosis, autophagy, and pyroptosis in CSFV infection and immunity in order to reveal the pathogenesis and immune escape mechanism of CSFV, which will have important guiding significance for the development of specific drugs and vaccines for CSF prevention, control, and eradication.…”

Section: Discussionmentioning

confidence: 99%

“…It has been found that there are three relationships between autophagy and apoptosis in the process of inducing cell death, including collaboration, antagonism, and promotion [83]. Gou et al found that autophagy and apoptotic signals were increased in the spleen of CSFV-infected piglets [84]. Interestingly, these autophagy-positive and apoptosis-positive cells were mainly distributed around splenic corpuscles.…”

Section: Cross-talk Between Apoptosis and Autophagy In Csfv Pathogenesismentioning

confidence: 99%

See 1 more Smart Citation

Apoptosis, Autophagy, and Pyroptosis: Immune Escape Strategies for Persistent Infection and Pathogenesis of Classical Swine Fever Virus

Mao

et al. 2019

Pathogens

View full text Add to dashboard Cite

Classical swine fever (CSF) is a severe acute infectious disease that results from classical swine fever virus (CSFV) infection, which leads to serious economic losses in the porcine industry worldwide. In recent years, numerous studies related to the immune escape mechanism of the persistent infection and pathogenesis of CSFV have been performed. Remarkably, several independent groups have reported that apoptosis, autophagy, and pyroptosis play a significant role in the occurrence and development of CSF, as well as in the immunological process. Apoptosis, autophagy, and pyroptosis are the fundamental biological processes that maintain normal homeostatic and metabolic function in eukaryotic organisms. In general, these three cellular biological processes are always understood as an immune defense response initiated by the organism after perceiving a pathogen infection. Nevertheless, several viruses, including CSFV and other common pathogens such as hepatitis C and influenza A, have evolved strategies for infection and replication using these three cellular biological process mechanisms. In this review, we summarize the known roles of apoptosis, autophagy, and pyroptosis in CSFV infection and how viruses manipulate these three cellular biological processes to evade the immune response.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Cross-talk Between Apoptosis and Autophagy In Csfv Pathogenesismentioning

confidence: 99%

Apoptosis, Autophagy, and Pyroptosis: Immune Escape Strategies for Persistent Infection and Pathogenesis of Classical Swine Fever Virus

Mao

et al. 2019

Pathogens

View full text Add to dashboard Cite

show abstract

“…During CSFV infection, the viral proteins NS5A and E2 colocalize with the autophagy marker CD63 on autophagosome-like vesicle membranes. Moreover, CSFV infection can use mitophagy to inhibit cell apoptosis to create a persistent environment for viral infection (Pei et al, 2016;Gou et al, 2017). However, the mechanisms underlying CSFVautophagosome entry are unclear.…”

Section: Introductionmentioning

confidence: 99%

Dual NDP52 Function in Persistent CSFV Infection

Fan

Luo

et al. 2020

Front. Microbiol.

Self Cite

View full text Add to dashboard Cite

Viruses have evolved many mechanisms to escape host antiviral responses. Previously, we found that classical swine fever virus (CSFV) infection induces autophagy using the autophagosome as a self-replication site, thereby evading the host immune response and promoting long-term infection. However, the underlying mechanisms used by CSFV to enter autophagosomes and the mechanism by which autophagy promotes viral replication remain unclear. We found that CSFV infection inhibited autophagy receptor nuclear dot protein 52 kDa (NDP52) expression, ubiquitination, and SUMO2-4 modification. Further analyses revealed that CSFV mediated ubiquitination and SUMOylation of NDP52 via Pten-induced kinase 1 (PINK1)-Parkin. Moreover, NDP52 inhibition also inhibited CSFV replication and the induction of mitophagy marker proteins expression. Inhibition of NDP52 reduced CD63 expression and binding to CSFV E2 protein, which has an essential role in persistent CSFV infection. As NDP52 has a close relationship with the NF-κB innate immunity pathway and plays an important role in the antiviral response, we investigated whether NDP52 inhibited CSFV replication through the release of immune factors and antivirus signals. Our results showed that inhibiting NDP52 boosted interferon and TNF release and promoted NF-κB pathway activation. In summary, we found that NDP52 inhibition not only reduces CSFV binding and entry into autophagic vesicles, but also inhibits CSFV replication by active NF-κB antiviral immune pathways. Our data reveal a novel mechanism by which NDP52, an autophagy receptor, mediates CSFV infection, and provide new avenues for the development of antiviral strategies.

show abstract

“…Former research showed that autophagy played an important role in the process of CSFV infecting host cells [28][29][30][31]. It has been reported that autophagy was induced in ST cells after CSFV infection, which is conducive to virus replication [28].…”

Section: Kegg Pathway Enrichment Analysis Of Sh3glb1mentioning

confidence: 99%

Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages

et al. 2019

Biotechnology & Biotechnological Equipment

View full text Add to dashboard Cite

Although SH3GLB1 is well known as an autophagy-related protein, its response mechanism to virus infection has yet to be determined. Through digital gene expression (DGE) profile analysis, we identified that SH3GLB1 may be a key gene responding to classical swine fever virus (CSFV) infection in porcine alveolar macrophages (PAMs). The present study found that the mRNA expression and the SH3GLB1 protein level in CSFV Shimen infected PAMs were significantly higher than those of mock-infected PAMs. Furthermore, confocal microscopy analysis suggested that SH3GLB1 was temporally co-localised with CSFV E2. These findings contributed in developing our understanding of the mechanism of CSFV infection.

show abstract

Autophagy induces apoptosis and death of T lymphocytes in the spleen of pigs infected with CSFV

Cited by 20 publications

References 50 publications

Apoptosis, Autophagy, and Pyroptosis: Immune Escape Strategies for Persistent Infection and Pathogenesis of Classical Swine Fever Virus

Apoptosis, Autophagy, and Pyroptosis: Immune Escape Strategies for Persistent Infection and Pathogenesis of Classical Swine Fever Virus

Dual NDP52 Function in Persistent CSFV Infection

Classical swine fever virus-Shimen infection upregulates SH3GLB1 expression in porcine alveolar macrophages

Contact Info

Product

Resources

About